Abstract 16273: Dynamic Starling Mechanism is Impaired in Patients With Heart Failure With Preserved Ejection Fraction Compared With Age-Matched Seniors, Even at Similar Left Ventricular End Diastolic Pressure
Introduction: The beat-to-beat dynamic Starling mechanism (DSM), the dynamic modulation of stroke volume (SV) due to breath-to-breath changes in LV end-diastolic pressure (LVEDP), reflects ventricular-arterial coupling. Although DSM is impaired in HFpEF, it is not clear whether this is due to high baseline LVEDP, or intrinsic cardiac dysfunction.
Hypothesis: We hypothesized that the DSM would remain impaired in patients with HFpEF compared with age-matched controls even at similar levels of LVEDP.
Methods: Right heart catheterization and Model-flow analysis of the arterial pressure waveform were performed while preload was manipulated using lower body negative pressure (LBNP) to alter cardiac filling pressure. To compare the DSM between the 2 groups (HFpEF: N=8, vs. control group: N=9) at similar level of LVEDP, hemodynamic parameters were compared in HFpEF patients during LBNP -15mmHg, and in age-matched controls during supine rest (PCWP: 9.5±2.6 vs. 10±2.1 mmHg, respectively, P=0.60). Spectral transfer function analysis between pulmonary artery diastolic pressure (PAD) representing LVEDP versus SV index was applied to obtain gain and coherence.
Results: There was a strong linear relationship between PCWP and PAD in both HFpEF and controls (R2=0.92). There was no difference in the coherence, confirming the reliability of the linear transfer function, between the 2-groups (HFpEF vs. control group: 0.72±0.06 vs. 0.80±0.17, P=0.16). Spectral power density (SPD) of PAD, the input variable of the DSM, in HFpEF patients was greater than controls (0.74±0.4 vs. 0.31±0.39 mmHg2, respectively, P=0.018). Conversely, SPD of SV index, the output variable of DSM, in HFpEF patients was the same as controls (0.27±0.24 vs. 0.24±0.30 (ml/m2)2, respectively, P=0.74). Moreover, the DSM gain (transfer function gain between PAD and SV index) was substantially lower in HFpEF patients than controls even at a similar level of PAD (0.47±0.20 vs. 1.0±0.43 ml/m2/mmHg, respectively, P=0.008).
Conclusions: The results of this study highlight that the dynamic Starling mechanism in HFpEF is markedly reduced with compared age-matched controls even at the same level of LVEDP, which likely reflects poor LV distensibility and impairment of ventricular-arterial coupling.
Author Disclosures: M. Hieda: None. E. Howden: None. J. Lawley: None. S. Satyam: None. D. Stoller: None. T. Urey: None. T. Tarumi: None. S. Shibata: None. Q. Fu: None. D. Palmer: None. R. Zhang: None. B.D. Levine: None.
- © 2016 by American Heart Association, Inc.